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Decrease of pancreatic somatostatin in neonatal nesidioblastosis.

A E Bishop, J M Polak, P G Chesa

    Diabetes
    |February 1, 1981
    PubMed
    Summary
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    Severe neonatal hypoglycemia and nesidioblastosis show a significant decrease in pancreatic somatostatin cells and content. This hormonal imbalance suggests a key role for somatostatin deficiency in the condition.

    Area of Science:

    • Endocrinology
    • Pediatric Pathology
    • Cell Biology

    Background:

    • Nesidioblastosis and severe neonatal hypoglycemia are characterized by inappropriate insulin release.
    • The role of B-cell proliferation was previously emphasized.
    • Somatostatin's potential role in regulating insulin release has only recently been considered.

    Purpose of the Study:

    • To investigate the levels of somatostatin cells and content in infants with nesidioblastosis.
    • To compare pancreatic hormone profiles in affected infants versus controls.

    Main Methods:

    • Immunocytochemistry and radioimmunoassay were used to analyze pancreatic tissue.
    • Insulin, somatostatin, and glucagon levels were quantified.
    • Tissue from five infants with nesidioblastosis and controls was examined.

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    Main Results:

    • No significant difference in insulin cell hyperplasia or insulin content was found between groups.
    • A significant decrease (over 50%) in somatostatin cells was observed in nesidioblastosis cases (P < 0.02).
    • Somatostatin content was significantly reduced by nearly 60% in affected infants (P < 0.01).

    Conclusions:

    • Nesidioblastosis is associated with a marked reduction in pancreatic somatostatin.
    • This somatostatin deficiency contributes to the altered pancreatic hormone balance in severe neonatal hypoglycemia.
    • Findings highlight the critical role of somatostatin in regulating insulin release in neonates.